H2A.Z Functions To Regulate Progression through the Cell Cycle

Abstract

Histone H2A variants are highly conserved proteins found ubiquitously in nature and thought to perform specialized functions in the cell. Studies in yeast on the histone H2A variant H2A.Z have shown a role for this protein in transcription as well as chromosome segregation. Our studies have focused on understanding the role of H2A.Z during cell cycle progression. We found that htz1Δ cells were delayed in DNA replication and progression through the cell cycle. Furthermore, cells lacking H2A.Z required the S-phase checkpoint pathway for survival. We also found that H2A.Z localized to the promoters of cyclin genes, and cells lacking H2A.Z were delayed in the induction of these cyclin genes. Several different models are proposed to explain these observations.

Supplemental material for this article may be found at http://mcb.asm.org/.

We thank Steve Bell, Doug Koshland, John Diffley, Paul Kaufman, Tom Petes, Judy Berman, Rodney Rothstein, Jasper Rine, Hiroyuki Araki, Judy Campbell, Mary Ann Osley, Rolf Sternglanz, Serge Gangloff, David Shore, Stefan Hohman, Akio Sugino, Peter Burger, Sue Biggins, Molly Fitzgerald-Hayes, Lorraine Pillus, Mary Bryk, Kim Nasmyth, David Stillman, Michael Grunstein, Carl Wu, Orna Cohen-Fix, Steve Elledge, and Munira Basrai for various plasmids, strains, and antibodies. We also thank Steve Bell, Doug Koshland, and John Diffley for protocols and technical help. We acknowledge help from the NCI FACS facility. We also thank Jasper Rine, Alan Hinnebusch, Mitch Smith, Munira Basrai, Lourdes Valenzuela, and Alex Strunnikov for helpful comments and suggestions.